Abstract

<h3>BACKGROUND</h3> Nitric oxide (NO) is known to modulate myocardial contraction and coronary tone, and its inhalation reduces pulmonary vascular resistance in patients with pulmonary hypertension. <h3>OBJECTIVES</h3> To evaluate the pathophysiological role of NO in patients with a ventricular septal defect (VSD). <h3>PATIENTS</h3> Twenty nine children with VSD, nine of whom had undergone VSD closure surgery, and 14 patients with Kawasaki disease. The mean age of the VSD patients was 3.1 years (range, 2 months to 9 years). <h3>METHODS</h3> Using high performance liquid chromatography, nitrate (a more stable NO oxidation product) was measured in plasma specimens of the patients undergoing cardiac catheterisation. <h3>RESULTS</h3> Nitrate concentrations in the pulmonary artery bore a significant relation to mean pulmonary artery pressure, pulmonary to systemic systolic pressure ratio, and pulmonary to systemic flow ratio. <h3>CONCLUSIONS</h3> The concentration of nitrate was in proportion to the increment in intravascular or cardiac pressure, indicating that endogenous NO is upregulated as a compensatory homeostatic attempt to reduce pulmonary pressure and blood flow. <h3>Key messages</h3> The concentration of nitrate in the pulmonary artery of VSD patients bears a significant relation to both the ratio of pulmonary to systemic systolic pressure (Pp/Ps) and the ratio of pulmonary to systemic flow (Qp/Qs) The concentration of nitrate in the pulmonary artery is reduced dramatically after surgery Plasma nitrate might be a good marker of intravascular pressure and pulmonary blood flow

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